Screening and follow-up of children exposed to tuberculosis cases, Luanda, Angola.

This prospective study enrolled children aged < 5 years with reported contact with adult tuberculosis (TB) patients in Angola. The study sample consisted of 124 children: 70 (56.5%) were active TB cases, 22 (17.7%) had latent TB infection (LTBI) and 32 (25.8%) were TB-exposed; 14 (20%) were human immunodeficiency virus positive. After 6 months of follow-up, 31.8% of the LTBI cases had evolved to active TB and 9.4% of the non-infected children had developed active TB. The strategy of simultaneous chest X-ray and TB skin test used in this study was effective; despite this protocol, however, 31.8% LTBI children developed active TB.

[Distribution and correlation of uric acid with classic cardiovascular risk factors in an adult population in Campania. VIP project data]. / Distribuzione e correlazione dell'acido urico con i classici fattori di rischio cardiovascolare in una popolazione adulta della Campania. I data del progetto VIP.

BACKGROUND: The aim of this study was to correlate uric acid levels with the classic cardiovascular risk factors in an adult population in Campania. METHODS: The following parameters were assessed in the study population (600 men and 600 women) aged between 25-74 years old, subdivided into 5 age groups (25-34, 35-44, 45-54, 55-64, 65-74): ECG, arterial pressure and body mass index (obtained by dividing weight in kg by height in metres squared). A blood sample was also taken to evaluate uric and other biochemical variables including: total cholesterol, HDL, L DI, glycemia, triglycerides, red and white blood cells, C3, fibrinogen, platelets and insulin serum levels. RESULTS: The results confirmed the positive correlation between uric acid and red and white blood cells in males, and between uric and the following variables in females: cholesterol, C3, LDL, systolic blood pressure, diastolic blood pressure, triglycerides, white blood cells, BMI and fibrinogen. When the correlation was performed in the entire population, uric acid correlated with triglycerides and red and white blood cells. Multivariate analysis for the entire population showed a strong correlation between uric acid, triglycerides and white blood cells. CONCLUSIONS: This study confirms the data reported in the literature and highlights the correlation between uric and the classic cardiovascular risk factors. This association is more evident in females.

Bradykinin release from high molecular weight kininogen and increase in plasma kallikrein-like activity following sensory stimulation by food in the rat.

Cephalic stimulation by food elicits, among other responses, dilatation of mesenteric blood vessels preparatory for digestion. The possible participation of bradykinin (BK), a powerful endogenous vasodilator, in this response was studied in fasted rats prior and following stimulation by sight and scent of food (sensory stimulation, SS), actual ingestion being denied to the animals. BK content of plasma high (HK) and low molecular weight kininogen (LK) was determined by bioassay on the atropinized, antihistamine-treated isolated guinea-pig ileum following release by trypsin from heat/acid denatured plasma. BK corresponding to LK was estimated in plasma which prior to denaturation had been incubated with kaolin, a process which leads to quantitative release and inactivation of BK from HK, but does not affect LK. BK corresponding to (HK + LK) was determined in plasma not exposed to kaolin. BK contained in HK was the difference between BK of (HK + LK) and of BK of LK. Plasma and glandular kallikreins were estimated by fluorimetry, using specific synthetic substrates. A 40.6+/-4.0% decrease (P<0.001) of BK in HK occurred in rats after 90 s of SS; LK remained unaffected. Ten minutes of SS did not result in further change. Atropine inhibited the effect of SS. Return of HK to pretreatment levels occurred when, following 90s of SS, rats were allowed to rest for 60 min in the absence of food. Renewed capacity to respond to SS was then observed. Plasma kallikrein, but not glandular kallikrein, increased in plasma of rats after SS. Increased free BK was detected in the circulation of Enalapril-protected rats after SS. Electrical stimulation of the distal sector of the sectioned left abdominal vagus nerve of Nembutal-anesthetized fasted rats reproduced the effect of SS on HK. It is concluded that visuo-olfactory stimulation by food generates nerve impulses, possibly carried by the vagus nerve, which by activating plasma kallikrein lead to cleavage of circulatory HK and release of BK in the rat.

Kininogen changes evoked in plasma by feeding, pseudo-alimentary, vagal and carbamylcholine stimulation of the rat.

Changes in plasma total (BKg), low (LKg), or high (HKg) molecular weight kininogens are indirect means of studying the participation of kinins in biological processes. To investigate kinin involvement in digestive activity, rats fasted overnight, but given access to water, were allowed to feed for one hour. BKg levels increased by 18% (p less than 0.0001); LKg by 29% (p less than 0.01); HKg remained apparently unchanged. Changes were reversed after 120 min. Decreases in circulatory HKg are probably masked by a compensatory response of the organism aimed at rapidly re-establishing kinin precursor levels in the circulation following their consumption by parasympathetic activity accompanying feeding. This conclusion is based on observations showing that fasted rats submitted to sham-feeding caused by visual/olfactory stimulation by food, present extensive (61%) reduction (p less than 0.001) of HKg, but not of LKg. It is further supported by results demonstrating that electrical stimulation of the distal stump of the cut left abdominal vagus nerve, as well as intravenous administration of carbamylcholine, a parasympathomimetic drug, also produce these changes, all of which were prevented by prior atropinization of the experimental animals. These results open the way for investigations on a possible role of kinins in the control of post-prandial vascular changes.

Stimulation of histamine synthesis in rat mast cells by compound 48/80 in vitro.

The histamine content of rat peritoneal fluid cells is doubled within 20 min by 0.5 microgram/ml of compound 48/80. Histamine catabolism inhibitors do not reproduce this effect; cells pre-incubated with alpha-fluoromethylhistidine are unresponsive to compound 48/80 which therefore activates pre-formed histidine decarboxylase rather than 'inducing' it. Non-mast cells showed no change after treatment with compound 48/80.